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Table1_Human_Illumina
Table2_Mouse_Illumina
Table3_Mse_Illumina_Nanopore
Table4_DESeq2_Hu
Table5_DESeq2_Mse
Table6_Differential_ATACseq
Table7_p65_irf3_peak
Table8_Mse_Homer_Aim2
Table9_Promoter_DAVID
Determining the layers of gene regulation within the innate immune response is critical to our understanding of the cellular responses to infection and dysregulation in disease. We identified a conserved mechanism of gene regulation in human and mouse via changes in alternative first exon (AFE) usage following inflammation, resulting in changes to isoform usage. Of these AFE events, we identified 50 unannotated transcription start sites (TSS) in mice using Oxford Nanopore native RNA sequencing, one of which is the cytosolic receptor for dsDNA and known inflammatory inducible gene, Aim2. We show that this unannotated AFE isoform of Aim2 is the predominant isoform transcribed during inflammation and contains an iron-responsive element in its 5′UTR enabling mRNA translation to be regulated by iron levels. This work highlights the importance of examining alternative isoform changes and translational regulation in the innate immune response and uncovers novel regulatory mechanisms of Aim2. ### Competing Interest Statement The authors have declared no competing interest.
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